期刊
NATURE COMMUNICATIONS
卷 9, 期 -, 页码 -出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/s41467-018-02938-1
关键词
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资金
- National Institutes of Health [CA191263, NS089641, NS083629, CA157948]
- NIH SIG grant [1S10OD019972-01]
- NIH/NCI [R00CA1606638]
- American Cancer Society [ACS127951-RSG-15-025-01-CSM]
- Komen [CCR15332826]
- Ohio Cancer Research Associates
- DOD Breast Cancer Research Program [BC150596]
- Clinical and Translational Science Collaborative of Cleveland [UL1TR000439]
- Case Comprehensive Cancer Center [P30 CA043703]
- Cleveland Clinic VeloSano Bike Race
- Sontag Foundation
- American Cancer Society
- Blast GBM
- Case Comprehensive Cancer Center
- CDMRP [BC150596, 893164] Funding Source: Federal RePORTER
Tumors adapt their phenotypes during growth and in response to therapies through dynamic changes in cellular processes. Connexin proteins enable such dynamic changes during development, and their dysregulation leads to disease states. The gap junction communication channels formed by connexins have been reported to exhibit tumor-suppressive functions, including in triple-negative breast cancer (TNBC). However, we find that connexin 26 (Cx26) is elevated in self-renewing cancer stem cells (CSCs) and is necessary and sufficient for their maintenance. Cx26 promotes CSC self-renewal by forming a signaling complex with the pluripotency transcription factor NANOG and focal adhesion kinase (FAK), resulting in NANOG stabilization and FAK activation. This FAK/NANOG-containing complex is not formed in mammary epithelial or luminal breast cancer cells. These findings challenge the paradigm that connexins are tumor suppressors in TNBC and reveal a unique function for Cx26 in regulating the core self-renewal signaling that controls CSC maintenance.
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